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Editorial
. 2015 Apr;22(4):519-21.
doi: 10.1038/cdd.2014.223.

Muscle gets stressed? p53 represses and protects

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Editorial

Muscle gets stressed? p53 represses and protects

L Latella et al. Cell Death Differ. 2015 Apr.
No abstract available

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Figure 1
Figure 1
Schematic representation of the DNA damage-activated networks contributing to the myogenic differentiation checkpoint. p53-mediated activation of the cyclin-dependent kinase inhibitor p21 promotes cell cycle arrest at specific checkpoints, to execute the DNA repair in myoblasts exposed to genotoxic agents. Simultaneous binding of p53 to the sequence RRRCWWGYYY (R=purine, W=adenine or thymine and Y=pyrimidine) located in one distal enhancer of myogenin gene represses myogenin transcription. In a parallel signaling, DNA damage-activated ABL tyrosine kinase inactivates MyoD transcriptional activity by phosphorylation of tyrosine 30 within the N-terminal domain, thereby inhibiting myogenin transcription. These two mechanisms of myogenin repression might relies on a common effector—the acetyltransferase p300/CBP—as p53 binding to myogenin enhancer decreases H3K27 acetylation (H3k27Ac) and ABL phosphorylates MyoD on a tyrosine residue previously implicated in the interaction with p300/CBP

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